Out of the 3 billion base pairs in the human genome , only about 2 % in reality tantalize for protein . Hidden in the vast chronological succession of non - coding deoxyribonucleic acid responsible for for inherited regulation are retroviruses that we have picked up throughout our evolutionary history . virus are usually match with disease , that is not always the case .
A new report provide evidence that some retroviral desoxyribonucleic acid became integrate in the neighborhood of the genome that influence regulation of gene in the brain , manipulating the cellular telephone ’ basic function . This could help explain why brainiac cells are able to have so many different part , and could even influence our intelligence or our susceptibleness to disease . The research team was headed by Johan Jakobsson of Lund University in Sweden , and the open access code paper was put out inCell Reports .
around 5 % of our desoxyribonucleic acid is believed to be attributed to these retroviruses ; most of which has been mix into non - coding DNA . Jakobsson ’s squad found that some endogenous retroviruses ( ERVs ) have become integrated into the regions creditworthy for regulating transcription ofneural primogenitor cells(NPCs ) . Nonproliferation Center are sort of like stalk cells , except they are only able to differentiate into different form of neurons . These ancient genetic stowaways are believed to actually play a part in regulating the function of genes in the brain .
" We have been able to observe that these viruses are activated specifically in the brain cells and have an important regulatory role , ” Jakobsson said in apress release . “ We believe that the part of retrovirus can lend to explicate why brain cells in finicky are so dynamic and multifaceted in their function . It may also be the case that the viruses ' more or less complex functions in various species can help us to understand why we are so different . ”
The corepressorTRIM28is a headmaster governor of ERVs as well as all other retroelements . Eliminating Trim28 in mouse lead in increase transcription of ERVs , which then began to affect locution of proximal genes . Targeting other ERV regulators could relent young information about how specific ancient hitchhikers influence genes in the brain , and what could potentially lead to their disfunction . sympathize the full effect that ERVs have on brain subroutine could have far-flung implications for diseases with a genetical component .
" I believe that this can lead to fresh , exciting study on the disease of the brain . Currently , when we count for genetic element linked to various diseases , we usually calculate for the genes we are familiar with , which make up a bare two per penny of the genome , ” Jakobsson explained .
“ Now we are unfold up the opening of looking at a much larger part of the genetic material which was previously debate unimportant . The double of the brain becomes more complex , but the area in which to search for error linked to diseases with a genetic component , such as neurodegenerative diseases , psychiatric illness and brain tumor , also increase . ”
